RAB32 promotes glioma cell progression by activating the JAK/STAT3 signaling pathway

• Published in: Journal of international medical research 2024-12, Vol.52 (12), p.3000605241282384
• Main Authors: Zhang, Sinan, Jiang, Xudong, Wei, Qing, Huang, Liji, Huang, Zhuoyan, Zhang, Lina
• Format: Article
• Language: English
• Subjects: Brain Neoplasms - genetics; Brain Neoplasms - metabolism; Brain Neoplasms - pathology; Cell Line, Tumor; Cell Movement - genetics; Cell Proliferation - genetics; Disease Progression; Female; Gene Expression Regulation, Neoplastic; Glioma - genetics; Glioma - metabolism; Glioma - pathology; Humans; Janus Kinases - genetics; Janus Kinases - metabolism; Male; Middle Aged; Neoplasm Invasiveness; Preclinical Study; Prognosis; rab GTP-Binding Proteins - genetics; rab GTP-Binding Proteins - metabolism; Signal Transduction; STAT3 Transcription Factor - genetics; STAT3 Transcription Factor - metabolism
• ISSN: 1473-2300; 0300-0605; 1473-2300
• DOI: 10.1177/03000605241282384

This study aimed to investigate the role of RAB32 in glioblastomas and its molecular mechanisms that regulate gliomas. The expression and prognostic value of RAB32 were evaluated using western blotting and the Gene Expression Profiling Interactive, Chinese Glioma Genome Atlas, and The Cancer Genome Atlas databases. Lentivirus containing sh-RAB32 or OE-RAB32 was used to manipulate RAB32 expression in glioma cells. The effects of RAB32 on cell proliferation, migration, and invasion were determined by western blotting, cell counting kit-8, plate cloning, wound healing, and transwell assays. Gene set enrichment analysis was used to screen for associations between the JAK/STAT3 signaling pathway and RAB32. The role of this pathway was verified using JAK/STAT3 inhibitors. RAB32 expression was significantly upregulated in patients with glioma and in glioma cell lines. The expression level was positively correlated with the glioma grade and served as an independent prognostic factor. In vitro experiments revealed that RAB32 knockdown inhibited glioblastoma cell proliferation, migration, and invasion, while the opposite effects were observed with overexpression and could be inhibited by the JAK/STAT3 inhibitor BP-1-102. RAB32 promotes malignant progression of glioblastoma cells through the JAK/STAT signaling pathway, providing new possibilities for therapeutic targets for glioblastoma.